tailieunhanh - Báo cáo khoa học: Reduced FAS transcription in clones of U937 cells that have acquired resistance to Fas-induced apoptosis

Susceptibility to cell death is a prerequisite for the elimination of tumour cells by cytotoxic immune cells, chemotherapy or irradiation. Activation of the death receptor Fas is critical for the regulation of immune cell homeo-stasis and efficient killing of tumour cells by apoptosis. | ỊFEBS Journal Reduced FAS transcription in clones of U937 cells that have acquired resistance to Fas-induced apoptosis Jeanette Blomberg Kristina Ruuth Maria Jacobsson Andreas Hoglund Jonas A. Nilsson and Erik Lundgren Department of Molecular Biology Umea University Sweden Keywords CpG methylation ERK activation by PD98059 Fas Fas expression TNF-a resistance Correspondence J. Blomberg Department of Molecular Biology Umea University S-90187 Umea Sweden Fax 46 90 771420 Tel 46 90 7852535 E-mail Received 16 July 2008 revised 6 November 2008 accepted 12 November 2008 doi Susceptibility to cell death is a prerequisite for the elimination of tumour cells by cytotoxic immune cells chemotherapy or irradiation. Activation of the death receptor Fas is critical for the regulation of immune cell homeostasis and efficient killing of tumour cells by apoptosis. To define the molecular changes that occur during selection for insensitivity to Fas-induced apoptosis a resistant variant of the U937 cell line was established. Individual resistant clones were isolated and characterized. The most frequently observed defect in the resistant cells was reduced Fas expression which correlated with decreased FAS transcription. Clones with such reduced Fas expression also displayed partial cross-resistance to tumour necrosis factor-a stimulation but the mRNA expression of tumour necrosis factor receptors was not decreased. Reintroduction of Fas conferred susceptibility to Fas but not to tumour necrosis factor-a stimulation suggesting that several alterations could be present in the clones. The reduced Fas expression could not be explained by mutations in the FAS coding sequence or promoter region or by silencing through methylations. Protein kinase B and extracellular signal-regulated kinase components of signalling pathways downstream of Ras were shown to be activated in some of the resistant clones but none of the three RAS .

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